Morphine and related opioids produce their major effects on the central nervous system and bowel. The effects of these compounds are diverse and include analgesia, drowsiness, changes in mood, respiratory depression, decreased gastrointestinal motility, nausea, vomiting, and alterations of the endocrine and autonomic nervous systems. Much research in the field of opioid pharmacology has focused on the understanding of the molecular nature of the phenomena of tolerance and physical dependence attendant to prolonged medical treatment with these compounds as well as the non-medical use thereof (such as in compulsive drug use or compulsive drug abuse).
Calcium has been hypothesized to play an important role in morphine-induced analgesia possibly due to the ability of morphine to inhibit calcium movement in nerve terminals (Kaimkubo et al, European Journal of Pharmacology, Vol. 95, p. 149, 1983). Some evidence is available which may tend to support this hypothesis. For example, in "Methods in Psychobiology", Vol. 2, pp. 155 et seq (1972), Weeks has described the ability of calcium channel blockers to produce morphine-like analgesia and Kakunaga et al (J. Pharmacol. Exp. Ther., 153, p. 134, 1966) describe their findings that calcium ions and calcium ionophores can elicit hyperalgesia. Additionally it has been reported that chronic treatment with opioids results in an increase in potassium-stimulated calcium uptake in brain synaptosomes (Calcium in Drug Action, J. B. Weiss, Editor, pp. 241 et seq, Plenum Press, New York, 1978). However, none of the research in opioid pharmacology has suggested that calcium channel blocking drugs may be useful in suppressing withdrawal symptoms in opioid-induced tolerant or physically dependent individuals.